Rheumatology Advance Access originally published online on April 27, 2004
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Rheumatology 2004; 43: 852-857
Rheumatology Vol. 43 No. 7 © British Society for Rheumatology 2004; all rights reserved
Concise Report |
Chondrogenesis of expanded adult human articular chondrocytes is enhanced by specific prostaglandins
1 Departments of Surgery and of Research, University Hospital and 2 M. E. Mueller Institute, Biozentrum, University of Basel, Basel, Switzerland.
Correspondence to: M. Jakob, Institute for Surgical Research and Hospital Management, University Hospital Basel, Hebelstrasse 20, ZLF, Room 405, 4031 Basel, Switzerland. E-mail: mjakob{at}uhbs.ch
Objective. To investigate the effects of the cyclooxygenase-2 (cox-2)-dependent prostaglandins D2 (PGD2), E2 (PGE2) and F2
(PGF2
) on the redifferentiation and cartilage matrix production of dedifferentiated articular chondrocytes.
Methods. Human articular chondrocytes from three adult donors were dedifferentiated by monolayer expansion and induced to redifferentiate by culture as 3D pellets in a defined serum-free medium containing TGF-ß1 and dexamethasone, without or with further supplementation with PGD2, PGE2 or PGF2
. After 2 weeks, pellets were assessed histologically, immunohistochemically, biochemically and by real-time quantitative reverse transcriptasepolymerase chain reaction.
Results. All three PGs, but predominantly PGE2, reduced the staining intensity of pellets for collagen type I, whereas PGD2 and PGF2
increased the staining intensity of pellets for collagen type II and glycosaminoglycans (GAG). The GAG/DNA content of pellets was not affected by PGE2 but was increased 1.5- and 2.1-fold by PGD2 and PGF2
respectively. PGE2 reduced the expression of collagen type I mRNA (9.0-fold), whereas PGD2 and PGF2
increased the mRNA expression of collagen type II (6.2- and 4.1-fold respectively) and aggrecan (29.8- and 10.7-fold respectively).
Conclusion. In contrast to PGE2, PGD2 and PGF2
enhanced chondrogenic differentiation and hyaline cartilage matrix deposition by expanded human articular chondrocytes, and could thus be used to improve in vitro or in vivo cartilage regeneration approaches based on these cells.
KEY WORDS: Tissue engineering, Cartilage repair, Cell differentiation, Cartilage degeneration, Joint inflammation